Pseudomonas aeruginosa, ubiquitous in nature, rarely produces disease in the normal host. However, Pseudomonas can invade a host when immunologic defenses are compromised either by diseases such as cystic fibrosis (CF), neoplastic diseases, and severe thermal injury or therapy treatments such as immunosuppressive agents or radiation therapy. In these instances of altered immune reactivity, Pseudomonas aeruginosa has emerged as a pathogenic microorganism of major importance becoming the major cause of morbidity and mortality among immunocompromised hosts. Two factors contribute to this high mortality: 1) the virulence of the organism and 2) the failure of the host defenses. Although the exact mode of pathogensis of P. aeruginosa has not been delineated, it appears that Pseudomonas extracellular products function as virulence factors in infection. It has also been established that microbes and their products can modulate the immune system by functioning as exogenous immunoregulatory agents. Taking these observations into consideration, this research effort is aimed at examining the mechanism by which Pseudomonas aeruginosa products interfere with the host's immune reactivity since immune reactivity of the host appears to be of major importance in the control of Pseudomonas infection. An in vitro cellular complementation system will be utilized which involves the use of nude mouse B-cells and macrophages to which various isolated and treated T-cells can be selectively added. In addition to resolving how Pseudomonas and its products may interfere with the natural regulated immune response, this complementation system will facilitate the testing of monoclonal cells lines representing the major classes of immunocytes. Moreover, these monoclonal cell lines provide stable cellular targets for analyzing the receptors involved in the binding of immunomodulatory microbial products.